COPD

Chronic Obstructive Pulmonary Disease encompasses two overlapping conditions: emphysema and chronic bronchitis. In emphysema, proteolytic destruction of alveolar walls by neutrophil elastase (amplified by alpha-1 antitrypsin deficiency or smoking-induced protease-antiprotease imbalance) destroys the elastic recoil of the lung parenchyma. Loss of alveolar septa reduces the surface area for gas exchange and eliminates the tethering effect that normally holds small airways open, causing expiratory airway collapse (air trapping). This creates enlarged airspaces distal to the terminal bronchioles with increased residual volume and total lung capacity (hyperinflation). In chronic bronchitis (defined clinically as productive cough for at least 3 months per year for 2 consecutive years), the pathology centers on airway inflammation with mucous gland hypertrophy (Reid index >50%), goblet cell hyperplasia, and excessive mucus production. Chronic inflammation causes bronchial wall thickening and smooth muscle hypertrophy, narrowing the airway lumen. Both processes contribute to V/Q mismatch: emphysema creates dead space (ventilation without perfusion - destroyed capillary bed), while chronic bronchitis and mucus plugging create shunt physiology (perfusion without ventilation). Chronic hypercapnia develops as the disease progresses, shifting the respiratory drive from CO2-mediated...